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    Toxicological evaluation of some food
    additives including anticaking agents,
    antimicrobials, antioxidants, emulsifiers
    and thickening agents



    WHO FOOD ADDITIVES SERIES NO. 5







    The evaluations contained in this publication
    were prepared by the Joint FAO/WHO Expert
    Committee on Food Additives which met in Geneva,
    25 June - 4 July 19731

    World Health Organization
    Geneva
    1974

              

    1    Seventeenth Report of the Joint FAO/WHO Expert Committee on
    Food Additives, Wld Hlth Org. techn. Rep. Ser., 1974, No. 539;
    FAO Nutrition Meetings Report Series, 1974, No. 53.

    SUCROSE ESTERS OF FATTY ACIDS, AND SUCROGLYCERIDES

    Explanation

         These substances have been evaluated for acceptable daily intake
    by the Joint FAO/WHO Expert Committee on Food Additives (see Annex 1,
    Ref. No. 20) in 1969.

         Since the previous evaluation, additional data have become
    available and are summarized and discussed in the following monograph.
    The previously published monograph has been expanded and is reproduced
    in its entirety below.

    BIOLOGICAL DATA

    SUCROSE MONOPALMITATE

    BIOCHEMICAL ASPECTS

         The ester linkage is only hydrolyzed with great difficulty by
    pancreatic or intestinal enzymes in vitro (Berry & Turner, 1960).
    The presence of sucrose monopalmitate had no effect on the absorption
    of Ca45 from aqueous CaCl2 solution when given intragastrically to
    six dogs. Estimation of blood activity up to six hours later showed
    only a delayed peak in the activity/time curve compared with plain
    aqueous CaCl2. Repetition in five dogs with induced impaired fat
    absorption secondary to ligation of the pancreatic duct showed higher
    Ca45 absorption postoperatively from the control solution and test
    solution containing sucrose monopalmitate. Giving intramuscular
    300 000 USP units of vitamin D decreased the blood levels in both
    cases but less so for the solution containing sucrose monopalmitate
    (Tudisco, 1961a, b).

    TOXICOLOGICAL STUDIES

    Acute toxicity

         Intragastric administration of 0.1 g to rats had no effect on the
    osmotic fragility of erythrocytes but intravenous administration to
    mice of 0.5 g/kg bw produced considerable haemolysis (Tudisco,
    1965a,b).

         An oral dose totalling 20 000 mg/kg, administered in 10 equally
    divided doses at 30 to 60 minute intervals produced no deaths in five
    rats (Tokita, 1958).

         An oral dose totalling 20 000 mg/kg, in 10 equally divided doses
    at 30 to 60 minute intervals, produced no deaths in 10 mice (Tokita,
    1958).

    Short-term studies

    Rat

         In another experiment groups of 10 male or female rats were given
    0, 1, 2, 3, 5, 10, and 25% sucrose monopalmitate for 100 days. At the
    2 and 3% levels (female rats used only) there was marginal reduction
    in body weight gain of the test groups. At the 5% level there were
    several deaths preceded by diarrhoea, weight gain was reduced but food
    efficiency high compared with controls. The 10% and 25% groups did not
    survive the first week and had white semi-soft faeces. Histopathology
    showed nothing of note (Tudisco; 1961a,b).

         Rats given daily oral doses of 100, 200, 1000, 2000 mg/kg for
    60 days grew normally and had normal organ weights (brain, heart,
    stomach, liver, spleen and kidney) at necroscopy (Hara, 1959).

    Dog

         Twelve male and 12 female young beagles were divided in four
    groups of three male and three female animals and fed a diet
    containing 0, 0.3, 1.0 and 3.0% sucrose monopalmitate for two years.
    Appearance, behaviour, appetite, elimination, body weight gains,
    urinalysis, organ weights, histopathology and organ function studies
    revealed no gross abnormalities or differences between test and
    control groups related to the compound (Hazelton Lab., 1966a).

    Long-term studies

    Rat

         Groups of 25 male and 25 female albino rats were fed dietary
    levels of 0.3, 1 and 3% sucrose monopalmitate for two years. The
    control groups consisted of 50 males and 50 females. There was one
    death in the first six months, a male in the 3% test group, apparently
    caused by bilateral pyelonephritis. Periodic records of body weight
    and food consumption disclosed a suggestion of lowered body weight
    gains in the 3% test groups. The first half-year growth rate and the
    78-week mean body weights of the 3% group females were significantly
    lowered; food consumption in the 3% group males was significantly
    lower at 26 weeks and slightly below that of controls in the first
    year; and the food efficiency of the 3% group females was slightly
    lowered in the first quarter year. No other differences were noted
    between the groups on the basis of observation of general appearance
    and behaviour, mortality and tumour incidence, haematology and
    urinalysis of pooled samples at 1, 3, 6, 12, 18 and 24 months, and
    sacrifice with necropsy, organ weight measurement and histological
    examination of tissues on five males and five females from each group
    at three months and of all survivors at 24 months (Hazelton Lab.,
    1966b).

         A concurrent reproduction study over three generations was
    carried out on groups of eight male and 16 female rats over 22 months
    using sucrose monopalmitate at 0 or 1% of the diet. The parent
    generation (P) was kept for the whole study. Mean body weight
    gain, survival and food consumption of the P generation showed no
    significant differences between controls and test group. The
    P generation was mated twice to give F1A and F1B filial generations.
    Of the F1A generation 10 male and 10 female pups were sacrificed for
    autopsy and the rest discarded. No significant findings were detected.
    The fertility index of the F1B test groups was significantly lower
    than that for the control groups due to adverse environment and
    unrelated to the test substance. Gestation, live birth and lactation
    indices were comparable between test and control groups. The F1B
    litter had slightly more frequent small weak pups with blue marks on
    the body but all survivors later developed normally. Sixteen F1B
    females and eight F1B males were mated twice to produce F2A and F2B
    filial generations, all other F1B animals were discarded including
    the 24 F1B animals used for mating. The F2A and F2B generation
    developed normally both in control and the test group. Growth of the
    males in the test group was slightly higher and for the females
    slightly lower otherwise control and test group showed no significant
    abnormalities. The F2A litter and all animals of the F2B litter
    except 16 females and eight males were discarded, the latter being
    mated twice to produce the F3A and F3B filial generations. Five
    males and five females of these 24 F2B animals were sacrificed. Gross
    and histopathology of all major organs revealed no significant
    abnormalities. The F3A and F3B litters showed no difference from
    previous generations or between the test group and controls. Mean
    litter size, physical appearance and growth of litter were comparable
    among test and control groups for each generation and among the three
    filial generations. The autopsies and histological examinations were
    normal (Hazelton Lab., 1965).

    SUCROSE MONOSTEARATE

    BIOCHEMICAL ASPECTS

         Surviving intestine has been shown capable of hydrolyzing the
    glucosidic linkage of sucrose monostearate to glucose and fructose at
    one-quarter of the rate of sucrose hydrolysis. alpha-amylase and
    gluco- or fructo-invertase were unable To hydrolyze sucrose
    mono-stearate. Liver homogenate, but not intestinal mucosa
    homogenates, could oxidize sucrose monostearate. Only pancreatic juice
    was able to hydrolyze the ester linkage to a moderate degree (Berry &
    Turner, 1960).

    TOXICOLOGICAL STUDIES

    Acute toxicity

    Mouse

         An oral dose of 20 000 mg/kg, administered in 10 equally divided
    doses at intervals of 30 to 60 minutes, produced no deaths in 10 mice
    (Tokita, 1958).

    Rat

         An oral dose totalling 20 000 mg/kg administered in 10 equally
    divided doses at intervals of 30 to 60 minutes produced no deaths in
    10 rats (Tokita, 1958).

    Short-term studies

    Rat

         Rats were given daily oral doses of 100, 200, 1000 and 2000 mg/kg
    for 60 days without deleterious effect on weight gain or relative
    organ weights (brain, heart, stomach, liver, spleen, kidney) (Hara,
    1959).

    Long-term studies

         None available.

    MIXED PALMITIC AND STEARIC ACID ESTERS OF SUCROSE

    TOXICOLOGICAL STUDIES

    Short-term studies

    Rat

         Daily doses of 3000, 4000 and 6000 mg/kg were administered orally
    to rats in groups of six for 33 days. There were no effects on weight
    gain and no histopathology (Tokita, 1959).

    SUCROSE MONOOLEATE

    BIOCHEMICAL ASPECTS

         Rat liver homogenates hydrolyzed the ester bond almost completely
    in 60 minutes without attacking the glucosidic linkage. alpha-amylase,
    lipase and dog pancreatin are similarly effective. Invertases only
    released 3 to 6% of the existing glucosidic links. Intestinal mucosa
    and liver homogenates were able to oxidize 0.1% of the substrate
    (Berry & Turner, 1960).

    TOXICOLOGICAL STUDIES

    Acute toxicity

         No data available.

    Short-term studies

    Rat

         Groups (unstated number) of rats received 0, 2, 5, 10 and 20% of
    ester in their diet for six months. On]y at the 20% level (0.09%
    dimethylformamide) was there retardation of growth compared with
    controls. Soft faeces or mild diarrhoea occurred initially with 10%
    and 20% test diets but animals later become tolerant. On return to
    normal diet there was rapid regaining of full body weight (Oshima &
    Kajiwara, 1960).

    Long-term studies

    None available.

    SUCROSE MONOLINOLENATE

    BIOCHEMICAL ASPECTS

         Five rats with either their thoracic duct cannulated or having
    a bile and lymph fistula were given intragastrically an aqueous
    suspension of sucrose ester or linolenic acid. Linolenic acid
    increased in the lymph within 24 hours. No linolenic acid was found in
    the bile of animals given the ester during 48 hours and it appeared
    only slowly after 72 hours in controls given linolenic acid. Rats with
    both bile and thoracic duct fistula showed a rise in the lymph content
    of linolenic acid within 24 hours and none in the bile even after
    72 hours. Thus lymphatic absorption of the linolenic acid moiety was
    demonstrated. The percentage linolenic acid absorbed was the same
    whether the sucroester or the free acid was administered (Tudisco &
    Turner, 1963).

    TOXICOLOGICAL STUDIES

    Acute toxicity

         None available.

    Short-term studies

         None available.

    Long-term studies

         None available.

    PALM OIL SUCROSE ESTERS

    BIOCHEMICAL ASPECTS

         When aqueous suspensions of palm oil sucrose esters were given
    intragastrically to rats after pyloric ligation there was no evidence
    of digestive hydrolysis up to eight hours. In vitro use of
    intestinal juice on a substrate containing 1% palm oil sucrose esters
    for six hours produced only negligible hydrolysis of the ester and
    glucosidic linkage. A metabolic balance study on 35 male and female
    rats using food containing 5% palm oil sucrose esters and determining
    the amounts of ester given, the residue in stomach, gut, excreta and
    left over in food showed some 75% as unaccounted and, therefore,
    metabolized. Skeletal development as a measure of calcium absorption
    was determined by measuring growth of rat tails in two groups of 10
    rats receiving daily 1 ml of 50% palm oil sucrose esters suspension
    for 10 weeks. Tail growth was more rapid in the test group during the
    first four weeks but later was not significantly different from
    controls (Balea et al., 1966).

    TOXICOLOGICAL STUDIES

    Acute toxicity
                                                                

    Animal    Route     LD50 mg/kg bw       Reference
                                                                

    Rat       Oral      > 30 000            Balea, 1963
                                                                

         Mice receiving intravenous doses of 1-2 g/kg bw showed no
    haemolysis (Tudisco, 1965a, b).

    Short-term studies

    Rat

         Groups of eight rats received 5% or 10% palm oil sucrose esters
    in their diet for 150 days without showing any deleterious effect on
    body weight gain (Tudisco & Chiancone, 1965). Three groups of 10 rats
    were fed diets containing 10 g/kg bw lard with either 0, 50 ml/kg bw
    10% palm oil sucrose esters and 10 ml/kg bw 50% palm oil sucrose
    esters for six weeks. No gastrointestinal disturbances were seen. Test
    groups showed a slightly greater body weight gain and slightly larger
    fat deposits in their carcass compared with controls (Balea et al.,
    1966). When the compound was fed to groups of eight males and eight
    female rats at 0, 3, 5, and 10% levels of their diet for 100 days no
    difference was noted between tests and controls regarding general
    condition. Test groups showed a slightly greater weight increase.

    Haematology, organ weights and gross autopsy were comparable in tests
    and controls, while histopathology revealed no abnormalities in the
    test group (Balea, 1963). In a similar experiment with 8-10 female
    rats per group, these received 0, 5 and 10% of the compound in their
    diet for 100 days. No abnormalities related to the test substance were
    detected in general appearance, food consumption, body weight gain,
    food efficiency, haematology, gross autopsy findings, histology
    (thyroid, liver, adrenal) and biochemistry (plasma and liver
    cholesterol, phospholipids, total lipids) only the liver lipids of
    test animals were significantly raised (Tudisco, 1963a).

         Two groups of 10 rats received 0 or 2% palm oil sucrose esters in
    their diet for three-and-one-half months. No deleterious effect was
    noted on mating, reproduction, litter number and litter size. Pups
    gained weight satisfactorily during weaning with better performance in
    the test group. Lactation was unaffected and no external fetal
    abnormalities were seen (Fernando, 1964).

    Long-term studies

    Rat

         Groups of 15 male or female rats were fed diets containing 0 or
    0.5% of the compound for 14 months. No tumours were seen at the end of
    13 months nor any growth abnormalities in male rats. Female rats
    showed a temporary lowering of growth rate during the eighth to tenth
    week. Three animals were examined histologically and no evidence of
    abnormality attributable to palm oil sucrose esters was found.
    Haematologic findings and blood proteins were comparable in test and
    control groups (Chiancone et al., 1963).

         Groups of 12 male rats were fed 0 or 10% of the ester as only
    source of lipids in their diet for 25 to 28 months. No abnormalities
    were found with respect to body weight, general health, mortality,
    haematology, plasma proteins and food efficiency. Tumour incidence was
    similar in test groups and controls. Visceral abnormalities were
    equally distributed (Tudisco & Chiancone, 1965).

         A two-generation study was carried out on 15 male and 15 female
    rats given 0 and 5 g/kg bw palm oil sucrose esters containing 68 ppm
    (0.0068%) of dimethyl formamide daily, The parent generation (P) was
    observed for two years. Body weight gain, external appearance and
    incidence of tumours were identical to controls. Three male animals
    died from intercurrent respiratory disease, three female animals
    either died or were sacrificed, the remaining 12 animals survived
    24 months. No haematological abnormalities were detected and blood
    proteins had a normal electrophoretic pattern. At autopsy no
    significant lesions were found in the test group which were not also
    found in the controls. Histology was similarly comparable for tests

    and controls. Five male and five female rats (P generation) were mated
    after nine months' treatment to produce 23 F1 generation animals. The
    F1 generation was observed for 21 months. Body weight gain was
    similar to controls and no spontaneous deaths or illnesses occurred.
    Five male and five female survivors were autopsied after 21 months. No
    evidence of malignant tumours or other significant abnormalities was
    found which differed from the controls. Five male and five female F1
    animals were mated after nine months to produce 30 F2 generation
    animals. The F2 generation was observed for 14 months. All litter
    mates gained weight identical to controls. Five male and five female
    F2 animals were autopsied after 14 months. No malignant tumours or
    other pathological conditions were found which did not also occur in
    the controls. No other significant abnormalities were seen. Seven from
    50 animals examined showed hepatic hyperfunction. No evidence of any
    adverse effects on fertility and fetal development was seen (Mosinger,
    1964b).

    LARD AND TALLOW SUCROSE ESTERS

    BIOCHEMICAL ASPECTS

         Each of four dogs aged five to six years were given
    intragastrically l131-labelled triolein in olive oil, oil/water
    emulsion and oil/water emulsion containing lard sucrose esters and the
    plasma activity determined as a measure of absorption. Each animal
    served as its own control, the administrations being separated by
    seven-day intervals. With olive oil peak absorption occurred after six
    hours with a fall between six and eight hours. The oil/water emulsion
    gave inconsistent patterns while oil/water emulsion with lard sucrose
    esters had a peak absorption of four hours and less abrupt fall during
    four to eight hours. Lard sucrose esters did not appear to interfere
    with intestinal fat absorption (Tudisco, 1961a, b).

         Calcium absorption using Ca45Cl2 was tested in eight dogs
    using aqueous CaCl2 solution. CaCl2 in oil/water emulsion and
    CaCl2 in oil/water emulsion with lard sucrose ester. All doses were
    administered intragastrically and blood activity determined
    subsequently. Each dog acted as its own control. The presence of lard
    sucrose ester had no consistent effect on Ca45 absorption (Tudisco,
    1961a. b).

         Each of four dogs aged one year received simultaneous
    l131-labelled triolein and CA45Cl2 either in oil/water emulsion
    and oil/water emulsion with lard sucrose esters. All doses were given
    intragastrically. Lard sucrose esters had no effect on the pattern
    of absorption. Experiments were repeated in young and old dogs with
    ligated pancreatic duct and administering intragastrically
    l131-labelled triolein in oil/water emulsions or oil/water emulsions
    with lard sucrose ester. Pre-and post-operative blood samples showed
    that no significant effect was exercised by the ester (Tudisco,
    1961a, b).

         As much as 100 g fat as lard sucrose ester may be administered to
    dogs and human subjects without producing plasma turbidity or an
    increase in excreted faecal fat (Berry & Turner, 1960). Humans have
    been maintained for short periods on this material as the sole source
    of dietary lipid (Tudisco, 1965a, b).

    TOXICOLOGICAL STUDIES

    Acute toxicity

         Rats tolerated doses of 5 g/kg bw lard sucrose ester every two
    hours up to a total of 15 g; 10 g/kg bw every two hours up to a total
    of 30 g produced diarrhoea and death from overdistension. Single doses
    of 3.8 g/kg bw in dogs had no effect. Rabbits tolerated 2.0 g/kg bw
    single doses without deleterious effects (Tudisco & Chiancone, 1965).
    Intragastric administration of 1 g to rats or 20% of the ester in
    their diet produced no osmotic fragility of erythrocytes. Rabbits
    given 3-6 g intragastrically also showed no osmotic fragility rise.
    Intravenous administration of 1-2 g/kg bw to mice had no haemolytic
    effect (Tudisco, 1965a, b).

         Single oral doses of lard sucrose ester (48% sucrose ester, 12%
    triglycerides, 21% diglycerides, 19% monoglycerides) were administered
    to four adult dogs aged four to six years as follows: 56 g lard
    sucrose ester, after a long interval 40 g refined lard, after a long
    interval 56 g lard sucrose ester and 40 g refined lard. Thus each
    animal served as its own control. No gastrointestinal disturbances,
    toxic symptoms or abnormal findings were discovered when blood sugar,
    total lipid, glyceride, cholesterol, phospholipid and percentage fatty
    acid composition were estimated. Plasma turbidity was lowest in the
    dog receiving the ester alone (Tudisco, 1963b).

    Short-term studies

    Rat

         Groups of 12 animals received 0, 5%, 10% and 25% lard sucrose
    ester daily in their diet for 15 days without adverse effects except
    that the test group at the 25% level showed reduced body weight gain
    (Tudisco & Chiancone, 1965).

         In another experiment groups of 12 rats each received for 200
    days 5%, 10% and 25% lard sucrose ester in their diet while controls
    received 3.6%, 7.7% and 18% lard. Body weight gain was reduced at the
    10% and especially the 25% levels. Food consumption and food
    efficiency were reduced at both the 10% and 25% level. No abnormal
    findings were seen in haematology, and clinical tests (blood glucose,
    plasma lipids, plasma proteins, liver lipids). There were no undue
    gastrointestinal symptoms. Only test animals at the 25% level were
    autopsied, there were no significant abnormalities in organ weights or

    histology of kidney, spleen, thyroid and adrenals. The liver showed
    frequent "steatosis" (Lepetit Lab., 1961). When male rats were given a
    diet containing 25% lard sucrose ester or 18% lard and 7% sucrose for
    200 days there was no adverse effect noticeable in body weight gain,
    food consumption, survival. Clinical findings which could not be
    ascribed to high fat diet were absent. Only the total liver fat of
    tests and controls was raised while the blood cholesterol of controls
    was also higher. Autopsy revealed no significant organ changes
    (Tudisco, 1967).

    Long-term studies

    Rat

         Groups of nine to 11 male rats were fed 3.6% lard, 5% and 10%
    lard sucrose ester in their diet as only source of lipids for 24 to 28
    months. No abnormalities were found with respects to body weight,
    general health, mortality or haematology. Tumour incidence was similar
    in test groups and controls. Visceral abnormalities were equally
    distributed (Chiancone et al., 1963, Tudisco & Chiancone, 1965).

         A two-generation study was carried out starting with 15 male and
    15 female rats receiving 0 and 5 g/kg bw lard sucrose ester containing
    52 ppm (0.0052%) of dimethyl formamide for two years. The parent
    generation was observed for two years. Four females died or were
    sacrificed for reasons unrelated to the test substance while 11
    animals survived. Three males died from respiratory disease. After 24
    months autopsies showed no malignant tumours or other conditions to be
    present which did not also occur to a similar extent in controls.
    Haematological findings were normal and electrophoresis or plasma
    proteins showed nothing unusual. Five males and five females were
    mated after nine months to produce 35 F1 generation pups. All F1
    animals gained weight satisfactorily without spontaneous deaths and
    were kept for 21 months. Five males and five females were examined
    after 21 months without showing any malignant or other tumours not
    also present equally in the controls. No abnormal findings were seen.
    Five males and five females of the F1 generation were mated after
    nine months to produce 32 F2 generation animals. The F2 generation
    survived for 14 months without showing any abnormalities as regards
    body weight gain or mortality. Five male and five female F2 animals
    were autopsied at 14 months without showing any unusual tumours of
    benign lesion or other condition not occurring equally frequently in
    the controls. No adverse effects were seen on fertility or fetal
    development (Mosinger, 1964a).

         Groups of 15 male or female rats were fed diets containing 0 or
    0.5% tallow sucrose ester for 14 months. No tumours were seen at the
    end of 13 months nor any growth abnormalities in male rats. Female
    rats showed a temporary lowering of growth rate during the eighth to
    tenth week. Three animals were examined histopathologically and no

    evidence of abnormality attributable to the ester was found.
    Haematology and blood protein investigation showed comparable results
    in tests and controls. No animal died (Oshima & Kajiwara, 1960).

    Comments:

         It seems reasonable, in evaluating these compounds, to consider
    mainly their metabolic fate in the animals studied provided that it is
    similar to their metabolic behaviour in man. However, the available
    metabolic studies are not adequate to reveal the pathways of
    individual products. The long-term feeding studies in rats on some
    representative compounds are adequate. A two-year study has been
    reported on sucrose monopalmitate. The presence of dimethyl formamide
    at levels up to 50 ppm (0.005%) has not introduced an adverse effect
    in the long-term toxicity tests on sucrose esters. However, most of
    the short-term and all long-term tests have been performed in the rat
    only.

    EVALUATION

    Level causing no toxicological effect

         Rat: 10 000 ppm (1%) in the diet equivalent to 500 mg/kg bw.

    Estimate of acceptable daily intake for man

         0-2.5* mg/kg bw.**

    FURTHER WORK OR INFORMATION

         Required by June 1976.

         Metabolic studies on representative individual sucrose esters.
    Two-year studies on another sucrose ester in a non-rodent mammalian
    species.

    REFERENCES

    Balea, T. (1963) Unpublished report from LARAC Laboratories

    Balea, T., Cariou, J. & Snozzi, C. (1966) Revue Franšaise des Corps
         Gras, No. 2, 3

              

    *    This applies to material the dimethyl formamide content of which
    does not exceed 50 ppm (0.005%).
    **   Temporary

    Berry, J. F. & Turner, A. D. (1960) J. Amer. Oil Chem. Soc., 37, 302

    Chiancone, F. M. et al. (1963) Ann. Fals. Exp. Chim., 56, 193

    Fernando, R. (1964) Unpublished report

    Hara, S. (1959) Submission to Japanese Ministry of Health and Welfare

    Hazelton Laboratories (1965) Report to Sucro-Chemical Division dated
         3 June 1965

    Hazelton Laboratories (1966a) Report to Sucro-Chemical Division dated
         25 March 1966

    Hazelton Laboratories (1966b) Report to Sucro-Chemical Division dated
         20 April 1966

    Lepetit Laboratories (1961) Unpublished report dated October

    Mosinger, M. (1964a) Unpublished report

    Mosinger, M. (1964b) Unpublished report

    Oshima, M. & Kajiwara, M. (1960) Takeda Kenkyusho Nempo, 19, 172

    Tokita, K. (1958 & 1959) Submissions to Japanese Ministry of Health
         and Welfare

    Tudisco, R. (1961) Unpublished report of Biochemistry Research
         Division, Dept. Medicine, Sinai Hospital, Baltimore

    Tudisco, R. (1961) Unpublished report to Lepetit Laboratories

    Tudisco, R. (1963a) Boll. Soc. ital. Biol. sper., 39, 1037

    Tudisco, R. (1963b) Boll. Soc. ital. Biol. sper., 39, 1914

    Tudisco, R. (1965) Il Farmaco, 20, 372

    Tudisco, R. (1965), Rass. Med. Sper., 12, 139

    Tudisco, R. (1967) Arzneimittel-Forsch. 17, 350

    Tudisco, R. & Chiancone, F. M. (1965) Third Congr. Naz. Stud. Alim.,
         Bologna

    Tudisco, R. & Turner, A. D. (1963) Boll, Soc. ital. Biol. sper., 39,
         1041


    See Also:
       Toxicological Abbreviations